ArticleCell reports2013
Human GEN1 and the SLX4-associated nucleases MUS81 and SLX1 are essential for the resolution of replication-induced Holliday junctions.
Article in Cell reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.
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Who cites it
95 citing papers in PubMed, 147 citations in OpenAlex.
- Trastuzumab deruxtecan in metastatic breast cancer with variable HER2 expression: the phase 2 DAISY trial.Nature medicine · 2023Trial
- CIP2A recruits SLX4-MUS81-XPF in mitosis and protects against replication stress.EMBO reports · 2026Article
- Mapping the genetic landscape of the DNA damage response with Cas12a-based combinatorial knockout screens.bioRxiv : the preprint server for biology · 2026Article
- Real-time visualization of spatial and temporal coordination in resolvase-mediated Holliday junction binding.iScience · 2026Article
- Dual-site phosphorylation of SLX4 stabilizes the SLX4-MUS81 interface to promote mitotic SMX assembly and genome protection.Nucleic acids research · 2026Article
- Mitotic errors as triggers of cell death and inflammation.Nature cell biology · 2026Review
- ANKLE1 processes chromatin bridges by cleaving mechanically stressed DNA.Nature communications · 2025Article
- RNF4 and USP7 coordinate spatial regulation of SLX4 stability within the PML nuclear bodies.Nucleic acids research · 2025Article
- ESSENTIAL MEIOTIC ENDONUCLEASE 1 is required for chloroplast development and DNA repair in rice.Plant biotechnology journal · 2025Article
- Homologous recombination promotes non-immunogenic mitotic cell death upon DNA damage.Nature cell biology · 2025Article
- Functional genetic variants of GEN1 predict overall survival of Chinese epithelial ovarian cancer patients.Journal of translational medicine · 2024Article
- Article
- The SUMO-NIP45 pathway processes toxic DNA catenanes to prevent mitotic failure.Nature structural & molecular biology · 2023Article
- Biochemical and mechanistic analysis of the cleavage of branched DNA by human ANKLE1.Nucleic acids research · 2023Article
- Human Endonuclease ANKLE1 Localizes at the Midbody and Processes Chromatin Bridges to Prevent DNA Damage and cGAS-STING Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Integrated transcriptomics and proteomics assay identifies the role of FCGR1A in maintaining sperm fertilization capacity during semen cryopreservation in sheep.Frontiers in cell and developmental biology · 2023Article
- STING in tumors: a focus on non-innate immune pathways.Frontiers in cell and developmental biology · 2023Review
- Sister chromatid exchanges induced by perturbed replication can form independently of BRCA1, BRCA2 and RAD51.Nature communications · 2022Article
- Pathogenic variants in SLF2 and SMC5 cause segmented chromosomes and mosaic variegated hyperploidy.Nature communications · 2022Article
- Article
35 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Holliday junctions (HJs), the DNA intermediates of homologous recombination, need to be faithfully processed in order to preserve genome integrity. In human cells, the BLM helicase complex promotes nonnucleolytic dissolution of double HJs. In vitro, HJs may be nucleolytically processed by MUS81-EME1, GEN1, and SLX4-SLX1. Here, we exploit human SLX4-null cells to examine the requirements for HJ resolution in vivo. Lack of BLM and SLX4 or GEN1 and SLX4 is synthetically lethal in the absence of exogenous DNA damage, and lethality is a consequence of dysfunctional mitosis proceeding in the presence of unprocessed HJs. Thus, GEN1 activity cannot be substituted for the SLX4-associated nucleases, and one of the HJ resolvase activities, either of those associated with SLX4 or with GEN1, is required for cell viability, even in the presence of BLM. In vivo HJ resolution depends on both SLX4-associated MUS81-EME1 and SLX1, suggesting that they are acting in concert in the context of SLX4.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.